2-Propenoic acid, heptadecyl ester, branched

Endpoint summary

Additional information

In vitro gene mutation assay on bacteria

This study was performed to investigate the potential of C 17 Acrylate dissolved in ethanol to induce gene mutations according to the plate incorporation test (experiment I) and the preincubation test (experiment II) using the Salmonella typhimurium strains TA 1535, TA 1537, TA 98, TA 100, and the Escherichia coli strain WP2 uvrA. The assay was performed with and without liver microsomal activation. Each concentration, including the controls, was tested in triplicate. The test item was tested at concentrations of 3; 10; 33; 100; 333; 1000; 2500; and 5000 μg/plate. Precipitation of the test item in the overlay agar on the incubated agar plates was observed from 1000 to 5000 μg/plate in experiment I with and without S9 mix and in experiment II without S9 mix. In experiment II with S9 mix precipitation was observed from 2500 to 5000 μg/plate. The undissolved particles had no influence on the data recording. No toxic effects, evident as a reduction in the number of revertants (below the indication factor of 0.5), occurred in the test groups with and without metabolic activation in both experiments. Only in experiment I a reduction in the number of revertants (below the indication factor of 0.5), was observed in strain TA 1537 from 1000 to 5000 μg/plates in the absence of metabolic activation. No substantial increase in revertant colony numbers of any of the five tester strains was observed following treatment with C 17 Acrylate at any dose level, neither in the presence nor absence of metabolic activation (S9 mix). Appropriate reference mutagens were used as positive controls and showed a distinct increase of induced revertant colonies.Therefore, C 17 Acrylate is considered to be non-mutagenic in this Salmonella typhimurium and Escherichia coli reverse mutation assay (BASF 2014).

In vitro chromosomal aberration assay on mammalian cells

The substance C 17 Acrylate was assessed for its potential to induce micronuclei in V79 cells in vitro (clastogenic or aneugenic activity). Two independent experiments were carried out, both with and without the addition of liver S9 mix from induced rats (exogenous metabolic activation). 1st Experiment 4 hours exposure, 24 hours harvest time, without S9 mix: 0; 12.5; 25.0; 50.0; 100.0; 200.0 μg/mL; 4 hours exposure, 24 hours harvest time, with S9 mix: 0; 12.5; 25.0; 50.0; 100.0; 200.0 μg/mL. 2nd Experiment 24 hours exposure, 24 hours harvest time, without S9 mix 0; 12.5; 25.0; 50.0; 100.0; 200.0 μg/mL; 4 hours exposure, 44 hours harvest time, with S9 mix 0; 12.5; 25.0; 50.0; 100.0; 200.0 μg/mL. The vehicle controls gave frequencies of micronucleated cells within our historical negative control data range for V79 cells. Both positive control substances, EMS and cyclophosphamide, led to the expected increase in the number of cells containing micronuclei. The test substance was poorly soluble in culture medium. In this study in the absence and the presence of metabolic activation no cytotoxicity indicated by reduced cell count or proliferation index (CBPI) was observed up to the highest applied test substance concentration, except in the 2nd Experiment in the absence of S9 mix where the concentration 100.0 μg/mL was not scorable due to low cell proliferation. In general, concentrations at the border of test substance solubility in culture medium were investigated for cytogenetic damage. On the basis of the results of the present study, the test substance did not cause any biologically relevant increase in the number of cells containing micronuclei either without S9 mix or after adding a metabolizing system. Thus, under the experimental conditions described, C 17 Acrylate is considered not to have a chromosome-damaging (clastogenic) effect nor to induce numerical chromosomal aberrations (aneugenic activity) under in vitro conditions in V79 cells in the absence and the presence of metabolic activation (BASF, 2015)

In vitro gene mutation assay in mammalian cells (read across, for justification see read-across document)

A GLP compliant HPRT assay is available for Behenylacrylate (Acrylate 22 45%) (Cas:4813-57-4; 48076-38-6; 18299-85-9) conducted according to OECD 476. The first main experiment was performed with and without liver microsomal activation and a treatment period of 4 h. The second experiment was performed with a treatment period of 24 hours in the absence of metabolic activation and 4 hours in the presence of metabolic activation. Chinese hamster lung fibroblasts (V79) were exposed (with and without S9 mix): 14.9, 29.7, 59.4, 118.8, 237.5, 475.0 µg/mL test substance in experiment I. Experiment II was conducted with (without S9-mix): 59.4, 118.8, 237.5, 475.0, 950.0, 1900.0 µg/mL and with S9-mix: 3.7, 7.4, 14.9, 29.7, 59.4, 118.8 µg/mL. No substantial and reproducible dose dependent increase of the mutation frequency was observed up to the maximum concentration with and without metabolic activation. Appropriate reference mutagens (EMS and DMBA), used as positive controls, induced a distinct increase in mutant colonies and thus, showed the sensitivity of the test system and the activity of the metabolic activation system. No relevant cytotoxic effects indicated by a relative cloning efficiency I or cell density below 50% in both parallel cultures occurred in any of the experimental parts with and without metabolic activation. In conclusion it can be stated that under the experimental conditions reported the test item did not induce gene mutations at the HPRT locus in V79 cells. Therefore, Behenylacrylate (Acrylate 22 45%) is considered to be non-mutagenic in this HPRT assay (Harlan, 2012).

A GLP compliant HPRT assay is available for 2-Propenoic acid, C12-14-alkyl esters (mixture of CAS no. 2156-97-0 and 21643-42-5) conducted according to OECD 476. Chinese hamster Ovary (CHO) were exposed to 0; 0.78; 1.56; 3.13; 6.25; 12.50; 25.00; 50.00; 100.00 μg/mL (without S9 mix, 4-hour ); 0; 3.13; 6.25; 12.50; 25.00; 50.00; 100.00 μg/mL (with S9 mix, 4-hour) in experiment I. Experiment II was conducted with 0; 0.78; 1.56; 3.13; 6.25; 12.50; 25.00; 50.00; 100.00 μg/mL (without S9 mix, 24 hour); 0; 1.56; 3.13; 6.25; 12.50; 25.0; 50.0; 100.0; 200.0 μg/mL (with S9 mix, 4-hour). In the 1st and 3rd Experiment in the absence and presence of metabolic activation, the highest concentrations tested for gene mutations were clearly cytotoxic. However, in the 2nd Experiment in the absence and presence of metabolic activation no cytotoxicity was observed up to the highest applied concentration. Therefore, a 3rd Experiment was performed which showed clearly reduced colony numbers at least at the highest concentrations. No substantial and reproducible dose dependent increase of the mutation frequency was observed up to the maximum concentration with and without metabolic activation. Appropriate reference mutagens (EMS and DMBA), used as positive controls, induced a distinct increase in mutant colonies and thus, showed the sensitivity of the test system and the activity of the metabolic activation system. In conclusion it can be stated that under the experimental conditions reported the test item did not induce gene mutations in CHO cells. Therefore, 2-Propenoic acid, C12-14-alkyl esters is considered to be non-mutagenic in this HPRT assay (BASF, 2012)

Justification for selection of genetic toxicity endpoint
Key study

Short description of key information:
Ames: negative (BASF, 2014)
MNT: negative (BASF, 2015)
HPRT in V79: negative (Harlan, 2012)
HPRT in CHO: negative (BASF, 2012)

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

Based on the results of the genetic toxicity testing, the test item was not classified and labelled according to Regulation (EC) No 1272/2008(CLP).